Effect of Banxia Xiexin decoction on Helicobacter pylori-related peptic ulcers and its possible mechanism via the TGF-β/Smad signaling pathway

Abstract

OBJECTIVE

To investigate the effect of Banxia Xiexin decoction (BXD) on Helicobacter pylori (Hp)-related peptic ulcers (PUs) and the possible mechanism underlying BXD actions via the transforming growth factor-β/small mothers against decapentaplegic (TGF-β/Smad) signaling pathway.

METHODS

PU patients with cold-heat complex syndrome were randomly assigned to groups that received Chinese or Western medicines with 20 patients in each group. Serum was collected after 7 d of treatment. The healthy group included 20 individuals. Gastric mucosal epithelial cell line GES-1 was cultured in vitro and randomly divided into the following seven groups: control, model, healthy, Western Medicine, prior treatment, low dosage, and high dosage. After 72 h of treatment with the corresponding serum, the mRNA and protein expression levels of TGF-β1, Smad3, and Smad7 were measured by reverse transcription quantitative polymerase chain reaction and western blotting, respectively.

RESULTS

The mRNA expression levels of TGF-β1 and Smad3 in GES-1 cells were increased after Hp introduction, and these increased levels were reduced by the BXD-containing serum. The protein levels of p-Smad3, but not TGF-β1 or Smad3, were significantly increased in Hp-treated GES-1 cells, and treatment with the BXD-containing serum markedly decreased the protein levels. Smad7 expression was significantly enhanced following treatment with the BXD-containing serum at transcriptional and protein levels in a dose-dependent manner.

CONCLUSION

BXD regulates the TGF-β/Smad signaling pathway by inhibiting the expression of TGF-β1 and Smad3, and increasing the expression of Smad7.